The demonstration of direct inhibitory actions of pharmacologic doses of somatostatin upon gastrointestinal function suggests the possibility that somatostatin may be a physiologic regulator of the rate of nutrient entry from the gut and thus provide the A-, B-, and D-cells with an influence over all avenues of nutrient flux. If so, the relative reduction in somatostatin-containing cells in the pancreatic islets of obese hyperglycemic mice might be responsible for some or all of the metabolic derangements of the obese hyperglycemic syndrome of mice, and conceivably its human counterpart as well. Hyposomatostatinemia would permit accelerated gastrointestinal function with more rapid entry of nutrients; higher postprandial nutrient levels would cause hyperinsulinemia and reduce the insulin sensitivity of glucoregulatory tissues. As hyperglycemia increased, the B-cell response to hyperglycemia would wane, further escalating the metabolic derangement. By contrast with the obese hyperglycemic syndrome, diabetes characterized by marked dimunution in B-cells is associated with an apparent augmentation of D-cells, perhaps reflecting a futile compensatory effort of D-cells to correct the hyperglycemia of insulin deficiency by inhibiting the entry rate of exogenous nutrients.
|Original language||English (US)|
|Number of pages||6|
|State||Published - Jun 15 1977|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
- Pharmacology, Toxicology and Pharmaceutics(all)